Sunday, October 19, 2025

Dopamine

Dopamine is a **dose-dependent catecholamine**: D₁/D₂ at low dose, **β₁ inotropy** at moderate dose, and **α₁ vasoconstriction** at high dose. 

It raises **CO** and **HR**, but carries **higher arrhythmia risk** than dobutamine/norepinephrine. 

Dose **2–20 mcg/kg/min**, central line preferred; **avoid** for “renal protection,” and **treat extravasation with phentolamine.


# 1) Receptor-level action → clinical effects


**Receptors (dose-dependent):**


* **D₁/D₂ (≈1–3 mcg/kg/min)** → renal/mesenteric vasodilation, natriuresis (the classic “renal dose” effect).

  **Clinical reality:** renal-protective strategy **not recommended**—no outcome benefit.

* **β₁ (≈3–10 mcg/kg/min)** → ↑ inotropy/chronotropy → ↑ CO, modest ↑ MAP.

* **α₁ (≥10–20 mcg/kg/min)** → vasoconstriction → ↑ SVR/MAP; tachyarrhythmia risk rises.


**Clinical effects from the above:**


* **Heart:** ↑ contractility (β₁), ↑ HR; may precipitate **AF/VT**.

* **Vessels:** low dose vasodilation (splanchnic/renal), moderate → little net change, high dose **vasoconstriction**.

* **Kidney:** ↑ diuresis at low dose in some, **but no proven renal protection**.

* **Metabolic:** can raise blood glucose, lactate (β-agonism).


---


# 2) Vial strength, preparation & basic PK (+ disadvantages)


**Supply / prep**


* Common vials/amps: **200 mg/5 mL** (40 mg/mL).

* Typical infusions: **200 mg/50 mL (4 mg/mL)** or **400 mg/50 mL (8 mg/mL)** in 0.9% saline or 5% dextrose. Use **central line** if possible; guard against extravasation.


**PK you feel at the bedside**


* **Onset:** 2–5 min; **peak** ~10 min.

* **Offset:** 5–10 min after stopping.

* **Metabolism:** MAO & COMT (hepatic, renal, plasma) → inactive metabolites.

* **t½:** ~2 min.


**Disadvantages (from PD/PK)**


* **Tachyarrhythmias**, ↑ myocardial O₂ demand, **variable BP response** (esp. hypovolaemia).

* High-dose **vasoconstriction** may impair splanchnic perfusion.

* **Less predictable** than norepinephrine; higher arrhythmia rates in shock.


---


# 3) Practical dosing


## A. Anaesthesia / OR (post-CPB or LV dysfunction)


* **Start:** **2–5 mcg/kg/min**, titrate q5–10 min by 2–5 mcg/kg/min.

* **Typical range:** **2–20 mcg/kg/min** (rarely higher).

* If hypotension with low SVR → may need **norepinephrine** adjunct rather than pushing dopamine high.


## B. ICU (shock, LCOS-Low Cardiac Output Syndrome)


* **Low cardiac output with relative bradycardia:** dopamine reasonable if you want **inotropy + HR** in one drug.

* **Septic shock:** **not first-line** (use **norepinephrine**); dopamine only if **bradycardic, low arrhythmia risk**, and limited access to other agents.

* **Cardiogenic shock:** can be used, but **arrhythmia risk > dobutamine**; many centres prefer **dobutamine ± norepinephrine**.


**Handy rate example (70 kg, 5 mcg/kg/min):**


* Using **8 mg/mL** (8000 mcg/mL): mL/h = (70×5×60) / 8000 ≈ **2.6 mL/h**.


---


# 4) Special populations — dosing cautions


### Pregnancy


* Use only if benefits outweigh risks (maternal shock). Can reduce uterine blood flow at high doses (α₁ vasoconstriction).


### Lactation


* Poor oral bioavailability; clinically minimal infant exposure with short maternal use.


### Hepatic impairment


* Metabolised by MAO/COMT widely (not solely hepatic). No strict adjustment; **titrate to effect**.


### Renal impairment


* Metabolites renally excreted; haemodynamics guide dosing. **Do not use** for “renal protection.”


### Obesity


* Start low; titrate to haemodynamic targets. (Most dose to **actual body weight**, but watch for excessive tachycardia.)


### Paediatrics


* **Start 2–5 mcg/kg/min**, titrate to 20 mcg/kg/min max under specialist monitoring (more arrhythmia-prone).


---


# 5) Drug interactions (clinically key)


* **MAO inhibitors** (or within 14 days): **massively potentiated** effect → severe hypertension/arrhythmias; **avoid or start at tiny doses with extreme caution**.

* **TCAs / SNRIs:** enhance pressor responses.

* **β-blockers:** blunt inotropy/chronotropy; unopposed α may ↑ SVR (context-dependent).

* **Inhalational anaesthetics (esp. halothane)**: **sensitise myocardium** to catecholamine-induced arrhythmias—use the lowest effective dose.

* **Other pressors/inotropes:** additive effects; coordinate with norepinephrine/dobutamine rather than stacking high dopamine alone.


---


# 6) Significant complications & management


| Complication                                       | Mechanism / Features                   | What to do                                                                                                                                                |

| -------------------------------------------------- | -------------------------------------- | --------------------------------------------------------------------------------------------------------------------------------------------------------- |

| **Tachyarrhythmias (AF/VT), myocardial ischaemia** | β₁ stimulation ↑ HR/O₂ demand          | Reduce/stop; correct electrolytes; consider **esmolol** (careful), switch to **dobutamine** or **norepinephrine** strategy.                               |

| **Hypertension with low output**                   | Excess α₁ tone                         | Titrate down; balance with inodilator (e.g., dobutamine/milrinone) if needed.                                                                             |

| **Extravasation → local ischaemia/necrosis**       | Intense α₁ vasoconstriction in tissues | **Stop infusion, leave cannula**, **infiltrate phentolamine 5–10 mg in 10–15 mL saline** around site ASAP; elevate/heat pack; surgical consult if severe. |

| **Gut/limb hypoperfusion** (high dose)             | Vasoconstriction                       | Lower dose; switch agent; ensure MAP/flow balance.                                                                                                        |

| **Endocrine effects (rare clinically)**            | Dopaminergic pituitary inhibition      | Usually not limiting; note possible ↓ prolactin transiently.                                                                                              |


---








No comments:

Post a Comment

How to Run Your Mind in a Cardiothoracic ICU Arrest

1. Do These First  1. Recognize fast.  2. Call early.  3. Start the standard ALS frame immediately.  4. Then, in parallel,  ask:  “Is this a...